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• W2153449310 startingPage "221" @default.
• W2153449310 abstract "An elevated level of oxidized LDL (ox-LDL) plays a crucial role in the development of atherosclerotic cardiovascular disease. LDL may be oxidized by reactive oxygen species in vivo. Ox-LDL stimulates the generation of reactive oxygen species through NADPH oxidase, increases oxidative stress and promotes foam cell formation by receptor-mediated uptake of ox-LDL. Ox-LDL is a potent agonist for the expression of multiple mediators involved in atherothrombosis. Plasminogen activator inhibitor-I (PAI-I), the major physiological inhibitor of plasminogen activators, is one of the inducible mediators implicated in both thrombogenesis and atherogenesis. Increased levels of PAI-I were detected in patients with atherosclerosis or diabetic cardiovascular complications. Heat shock factor-I (HSFI) is the key mediator for stress response-related proteins. Our recent studies demonstrated that HSFI is implicated in ox-LDL-induced upregulation of PAI-I gene in vascular endothelial cells. Lectin-like ox-LDL receptor-I, NADPH oxidase, H-Ras, protein kinase C-β and Raf-I/ERKI/2 pathway are involved in ox-LDL-induced HSFI and PAI-I upregulation in endothelial cells. ox-LDL-induced PAI-I production in vascular endothelial cells is one of the cellular responses to oxidative stress that contribute to atherogenesis and thrombosis." @default.
• W2153449310 created "2016-06-24" @default.
• W2153449310 creator A5054061739 @default.
• W2153449310 creator A5057501090 @default.
• W2153449310 date "2010-04-01" @default.
• W2153449310 modified "2023-09-26" @default.
• W2153449310 title "Signaling mechanisms for oxidized LDL-induced oxidative stress and the upregulation of plasminogen activator inhibitor-I in vascular cells" @default.
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